The document provides information on the basal ganglia including its history, neuroanatomy, pathways, connections, and related disorders. It describes the major structures of the basal ganglia such as the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra. It explains the direct and indirect pathways within the basal ganglia and how they regulate movement. Disorders associated with basal ganglia damage or pathology include Parkinson's disease, Huntington's disease, and Wilson's disease.
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
Largest part of hind brain.
Called “ silent area/Little Brain ”
Weight- 150 gms.
Cerebellar cortex is a large folded sheet, each fold is called Folium.
Connected to brain stem by 3 pairs of peduncles- Superior (Brachium conjunctiva), Middle (Brachium Pontis) & Inferior (Restiform body) peduncle.
The term basal nuclei is applied to a collection of masses of gray matter situated within each cerebral hemisphere.
They are the
corpus striatum,
amygdaloid nucleus,
claustrum.
The subthalamic nuclei, the substantia nigra, and the red nucleus are functionally closely related to the basal nuclei.
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
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Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
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Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
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Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
The prostate is an exocrine gland of the male mammalian reproductive system
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Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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NEURO-ANATOMY OF BASAL GANGLIA AND ITS CLINICAL IMPLICATIONS
1.
2. Brief History and Nomenclature
Neuro-anatomy of Basal Ganglia
Internal Processing (Direct and Indirect pathways)
Functional connections of Basal Ganglia
Disorders assoc. with damage to Basal Ganglia
Disorders assoc. with pathology of Basal Ganglia
Summary
References
3. First clear identification of subcortical structures was published
by anatomist Thomas Willis in 1664.
Basal Ganglia was then referred to as Corpus striatum.
The term “Corpus striatum” was coined by anatomists Cecile &
Oskar Vogt.
Detailed descriptions of Corpus straitum were given by Cajal &
Samuel Wilson.
Substantia nigra was first described by Von Sommering.
Subthalamic nucleus was first described by Jules Bernard Luys.
4. By definition, Ganglion is collection of neuronal cell
bodies outside the CNS and Nuclei are collection of cell
bodies within CNS surrounded by white matter.
So, term Basal Ganglia is a misnomer and they should
be actually called “Basal Nuclei.”
Basal Ganglia (Nuclei) are set of deep nuclei (grey
matter) located in and around the basal part of brain
and are involved in motor control, action selection and
some forms of learning.
5. Major Structures:
Caudate nucleus
Putamen
Globus pallidus
(Internal & External)
Subthalamic nuclei
Substantia nigra
Other Structures:
Ventral striatum
Ventral pallidum
(also k/a Neurological or Functional classification)
7. Telencephalic in origin
C-shaped structure
Divided into 3 parts:
Head, Body andTail
Head is continuous
with putamen
Tail terminates in the amygdala of temporal lobe
Assoc. with contour of lateral ventricles
(Head lies against frontal horn and tail lies against temporal horn)
8. Telencephalic in origin
Bounded laterally by external capsule, medially by Globus
pallidus
Separated by Caudate by fibres of anterior limb of internal
capsule
9. Diencephalic in origin,
also k/a Paleostriatum
or Pallidum
Inner component of
lentiform nucleus
Cone like structure with tip directed medially
Bounded medially by posterior limb of internal capsule and
laterally by putamen
Divided into external and internal segments by medial mamillary
lamina
10. Diencephalic in origin
Lies dorso-medially to
posterior limb of
internal capsule
Situated dorsal to
substantia nigra
Discrete lesions will
lead to Hemiballism
11. Mesencephalic in origin
It is present in mid-brain
(between tegmentum
and basis pedunculi)
It consists of
2 components:
-Pars Compacta
-Pars Reticulata
12. Dorsal cell rich portion
Most of the neurons are pigmented due to the presence of
Neuromelanin
Contains neurotransmitter Dopamine
Contain low levels of m-RNA for DA transporter and D2 receptor
Contains Calbindin (calcium binding protein)
Sends projections to areas of striatum dominated by input from
limbic related structures and association regions of cerebral
cortex.
May be associated in patho-physiology of Schizophrenia.
13. Ventral cell sparse portion
Uses neurotransmitter GABA
Contains higher levels of m-RNA for DA transporter and D2
receptor
Lacks Calbindin
Sends axonal projections to sensori-motor regions of striatum
May be associated in patho-physiology Parkinson’s disease
14. Ventral Striatum: Includes nucleus accumbens, which
is the region where Putamen and Head of Caudate
nucleus fuse. It is involved in cognitive and behavioral
functions.
Ventral Pallidum: receives afferents Ventral Striatum
and contains a group of neurons k/a Substantia
Innominata.
15. Majority of neurons in striatum are medium spiny
neurons (medium sized 10 -20 um in diameter).
Medium aspiny neurons, large spiny neurons and large
aspiny neurons are also found in striatum.
In striatum, AchE-rich zones k/a matrix are surrounded
by AchE-poor zones k/a striosomes.
Similar distribution is also found for Enkephalin,
Substance P and Somatostatin.
16. Striatum is major recipient of inputs to Basal Ganglia
There are 3 major afferent pathways that terminate
into the striatum:
-Cortico-striatal
-Nigro-striatal
-Thalamo-striatal
17. Originates from all regions of neo-cortex, primarily from frontal
and parietal areas (pyramidal cells of layerV andVI)
Uses excitatory neurotransmitter: Glutamate
Afferents from sensori-motor cortex terminate predominantly in
the putamen whereas afferents from association regions of
cortex preferentially terminate in the caudate nucleus.
Afferents from limbic cortex , the hippocampus and the amygdala
terminate in the ventral striatum
18. Arises from Substantia nigra Pars compacta
Uses neurotransmitter Dopamine
Different portions of striatum receive input from dorsal-tier or
ventral-tier DA containing neurons of Substantia nigra.
19. Originates in the thalamus
The thalamic nuclei providing the projections are intra-laminar
nuclei, particularly the central median nucleus
20.
21.
22. Striatum receives major projection from cerebral cortex
Within striatum, medium spiny neurons (containing
neuropeptide Substance P) sends inhibitory projections to
Globus Pallidus internal (Gpi).
23. Direct pathway reduces inhibitory output of Basal Ganglia
(Excitatory).
Consequence is to promote movement.
24. A subpopulation of these medium spiny neurons (containing
neuropeptide Enkephalin) provides inhibitory projections to
Globus pallidus external (Gpe) which sends inhibitory afferents
to Gpi.
25. Gpe projects to Substantia nigra reticulata.
Gpe also sends inhibitory projections to Subthalamic nucleus.
However neurons in Subthalamic nucleus provide excitatory
projections to Gpe, Gpi and Substantia nigra reticulata.
Indirect pathway increases inhibitory output of Basal Ganglia.
Consequence is inhibition of movement.
26. Dopamine released by Substantia nigra Pars Compacta:
Stimulates direct pathway via D1 receptor.
Inhibits indirect pathway via D2 receptor.
Hence, Dopamine promotes movement.
27. Gpi is the source of much of the output of Basal Ganglia.
Gpi provides projection to the ventral lateral(VL) and ventral
anterior (VA) nuclei of thalamus and the central median nucleus
(CM).
The substantia nigra pars reticulata also provides projections to
VL andVA nuclei.
These projections of VA and VL project to pre-motor and pre-
frontal cortices.
Projections of pre-motor & pre-frontal cortices project to primary
motor cortex, so Basal Ganglia are able to influence indirectly the
output of primary motor cortex.
28.
29. Cortical projections are to the Putamen > Gp> STN> Primary
motor, supplementary motor and Pre-motor area.
Functions in association with cortico-spinal system to controls
complex patterns of motor activity:
-Writing, cutting paper with scissors, hammering nails
-Movements like passing a football, throwing a baseball
-Most aspects of vocalisation
- Controlled movements of eyes
Virtually any other skilled movements, most of them performed
subconsciously.
30. Cortical projections are to the caudate.
Most motor actions occur as consequence of sensory input and
memory; k/a Cognitive control of motor activity.
Timing and scaling of movement
33. Tremors
Regular oscillating movement about a joint d/t synchronous
contraction of agonist and antagonist muscles resulting from
disequilibrium between Acetylcholine and Dopamine activity in
striatum.
1. Rest Tremor: movement occurs in a relaxed supported
extremity, reduced by ambulation.
2. Postural Tremor: Sustained posture elicit tremor e.g.:
Outstretched hand
3. Intention Tremor: Active limb oscillates more prominently when
reaching target e.g.: patient trying to touch examiner’s finger.
34. Chorea
Rapid semi-purposeful, graceful, dance like non patterened
involuntary movements involving distal or proximal muscle
groups due to involvement of caudate nucleus and degeneration
of GABA-ergic fibres.
Dystonia
Sustained or repititive involuntary muscle contractions
frequently causing twisting movements with abnormal postures
due to lesions in putamen circuit.
35. Athetosis
Slow, writhing, involuntary movements with a
propensity to affect arms and hands primarily due to
lesion of lenticular nucleus.
Hemibalismus
A violent form of chorea that comprises wild, flinging,
large amplitude movements on one side of the body,
contralateral to the lesion in subthalamic nuclei.
37. Neurodegenerative disease associated with loss of dopaminergic
neurons in SNPc accompained by loss of dopamine terminals in
striatum.
Decreased dopaminergic activity on both direct and indirect
pathways will lead to difficulty in initiation of movement resulting:
Hypokinesia, person walks slowly with little steps and stooped
posture and face looks like mask.
Decreased activity of cortico-reticular fibres will increase tone of
muscles leading to rigidity (rigid lead pipe limb).
Disequilibrium between Acetylcholine and Dopamine will result in
tremors.
38. Chorea results due to damage to GABA-ergic and
Cholinergic neurons (Inhibitory pathway) that project
into the putamen which releases the inhibition resulting
in hyperkinetic choreiform movements.
39. Autosomal recessive disorder in which mutations in the
gene atp7b, ceruloplasmin is low in blood resulting
abnormal copper accumulation in liver, basal ganglia
and other tissues.
When cu deposits in basal ganglia esp. in lentiform
nucleus, there is cell death.
Neurological manifestations: Tremors, Dystonia,
Rigidity, Bradykinesia, Choreoathetosis, Masked facies,
Micrographia.
40. Major Depressive Disorder: Hyperintensities in sub-cortical
regions such as Basal ganglia, Thalamus and periventricular
regions.
Tourette’s Disorder: Diffuse process involving CSTC
pathways.
OCD: Traumatic and infectious lesions of Basal ganglia,
advanced studies shows metabilic abnormalities in various
circuits of basal ganglia particularly in caudate.
ADHD: Evidence suggesting functional and anatomocal
dysfunction in frontal cortex and basal ganglia, CSTC circuit.
42. The Basal Ganglia are a group of subcortical nuclei of
varied embryonic origin.
Basal Ganglia includes Caudate nucleus, Putamen,
Globus pallidus, Subthalamic Nuclei and Substantia
nigra.
Main functions of Basal ganglia are Initiation and
Execution of complex patterns of motor activity and
cognitive control of motor patterns.
43. Abnormalities of Basal ganglia results in various
abnormal involuntary movements.
PD, Parkinsonian syndromes, Huntington’s Disease,
Wilson’s disease are important clinical syndromes
resulting from damage to Basal ganglia.
The importance of Basal ganglia from the Psychiatric
aspect is in the development of Neuroleptic induced
movement Disorders.
44. Kaplan and Sadock’s ComprehensiveTextbook of
Psychiatry
Snell’s Clinical Neuroanatomy
Guyton and Hall’s Medical Physiology
Lishman’s Organic Psychiatry
Adams andVictors Principles of Neurology
Internet, Google Scholar